(1) Canadian Blood Services,Vancouver, British Columbia, Canada (2) University of British Columbia, Department of Pathology and (3) Department of Psychiatry, Vancouver, British Columbia, Canada

Summary

Clinical depression has been proposed to be an independent
risk factor for cardiovascular disease. While it is suggested that
selective serotonin reuptake inhibitors (SSRIs) reduce the risk
of acute cardiovascular problems of depressed patients, the
effect of SSRIs on platelets, the only blood cells committed to
serotonin (5-HT) transport, remains largely unknown.The goal
of this pilot study was to measure the 5-HT levels in platelets
of untreated and SSRI-treated depressed patients and normal
subjects and to determine whether the interaction of SSRIs
with platelets can explain their possible cardiovascular benefit
in patients with depression. Platelet 5-HT was determined
by an immunocytochemical assay and high-pressure liquid
chromatography with electrochemical detection (HPLC-ECD).
In normal control subjects without cardiovascular disease, 78 ± 8% of platelets were 5-HT-positive (n = 14). Depression
caused a significant reduction in platelet 5-HT to 46 ± 21% in
untreated patients (n = 13) and 22 ± 13% in SSRI-treated
patients (n = 14). As a class, all selective serotonin reuptake
inhibitors significantly reduced the 5-HT concentration in
patient platelets. An inverse relationship of 5-HT level and dose
of medication might be suggested.These results correlated well
with 5-HT data from HPLC (r = 0.8509, p < 0.001). SSRIs did
not affect platelet aggregation and dense granule release in
response to thrombin, but significantly reduced ADP-induced
platelet aggregation and dense granule release in both patient
and normal control samples. The active inhibition of platelet
aggregation by SSRIs might explain their cardiovascular benefit.